论文部分内容阅读
目的探索微小胃癌实验引发的较好方法,观察分析微小胃癌的组织发生,阐明胃粘膜异型增生的癌前意义。方法低剂量(100μg/ml)致癌剂N-甲基-N’-硝基-N-亚硝基胍(MNNG)自由饮用,结合胃粘膜损伤(40%酒精灌胃,每次1.5ml,每周2次)共20周,引发微小胃癌。结果在实验组131只大白鼠中,得到胃腺癌33例,明显高于未给损伤的致癌剂对照组(P<0.01),其中微小胃癌4例(微小胃癌诱发率为12.12%)微小癌灶7灶。微小胃癌发生于胃固有层,起始于幽门腺区腺管颈部及小凹底部的干细胞。表现为单一的胃型胃癌。其组织类型均为高分化管状腺癌。结论低剂量致癌剂结合胃粘膜损伤可以增加胃癌诱发率,是一种较好的微小胃癌实验引发的方法;从胃癌始发阶段分析,胃粘膜异型增生的各种形态均有重要的癌前意义,其中再生型异型增生的癌前意义应被重新认识和重视。
Objective To explore the better methods induced by the tiny gastric cancer experiment, observe and analyze the histogenesis of tiny gastric cancer, and elucidate the precancerous meaning of gastric dysplasia. Methods The low-dose (100μg/ml) carcinogen N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) was freely administrated and combined with gastric mucosal injury (40% ethanol, 1.5ml each time, Twice a week for 20 weeks, causing microscopic gastric cancer. RESULTS: Among the 131 rats in the experimental group, 33 cases of gastric adenocarcinoma were significantly higher than those in the non-injured carcinogen control group (P<0.01). Among them, 4 cases of tiny gastric cancer (12.12% of tiny gastric cancer inducing rate). ) Microfoci 7 foci. Microscopic gastric cancer occurs in the gastric lamina propria, originating from the stem cells of the pyloric glands, the neck of the glands, and the bottom of the fovea. A single gastric stomach cancer manifests itself. Its tissue type is highly differentiated tubular adenocarcinoma. Conclusion Low-dose carcinogens combined with gastric mucosal injury can increase the gastric cancer inducing rate, which is a better method for the initiation of tiny gastric cancer experiments. From the analysis of the initial stages of gastric cancer, various forms of gastric dysplasia have important precancerous significance. The precancerous significance of regenerative dysplasia should be re-recognized and valued.